The Invest in ME Research conference took place on Friday,
2nd June, 2017.

This year’s conference was held
at One Great George Street, an impressive Edwardian building located opposite
St James’s Park, London. There was an excellent mixture of people with ME/CFS,
carers and parents, charity representatives, health professionals and
researchers from all over the world.

There was an emphasis on
immunology and new approaches to research that are aimed at increasing our
understanding of the underlying disease process in ME/CFS and research to
potentially deliver more effective forms of treatment.

Presentations covering treatment
were largely focused on the clinical trials taking place in Norway into the use
of rituximab and cyclophosphamide.

* This is a copy of the
conference summary that was published in the Autumn issue of ME Essential
magazine

* We have made Dr Shepherd’s full
(16-page) conference report available as a download, which might make it easier
for people with M.E. to read at their own pace

Summary review

Chairman, Dr Ian Gibson opened
the meeting with some quotes from a letter written by Sir Bruce Keogh, National
Medical Director at NHS England, relating to discussions that are currently
taking place at NICE. Current NICE guideline recommendations relating to CBT
and GET were referred to in this letter.

Professor Ian Charles of the
Quadram Institute of Food Health, University of Norwich: Prof. Charles spoke
about the important overlap between food and health and the role of the
microbiome in helping to regulate the body’s immune system and the signalling
systems that link the brain and gut. He explained how research is starting to
provide new insights about possible causal mechanisms in diseases such as
diabetes and obesity.

Dr Vicky Whittemore, Programme
Director, National Institutes of Neurological Disorders and Stroke at NIH, USA:
Dr Whittemore explained how the NIH (National Institutes of Health) operates
and talked about how it funds research. There are 27 separate institutes and
centres at NIH, each with a specific researchagenda focused on diseases or body systems and, as ME/CFS is an illness
that covers a wide range of symptoms and body systems, it now has 24 different
homes at NIH! NIH is also setting up a ME/CFS Data Management Co-ordinating
Centre and arranging educational seminars on ME/CFS.

Professor Donald Staines,
National Centre for Neuroimmunology and Emerging Diseases, Griffiths
University, Australia: The presentation focused on the work that Professor
Staines and his team have been doing at a molecular level on calcium ion
channels and cellular signalling mechanisms that involve calcium ions. This is
a process that could link in with some of the immune system disturbances found
in ME/CFS. It is possible that disturbances in the way that calcium ions are
behaving in ME/CFS could form part of the underlying disease process.

Professor Nancy Klimas, Director,
Institute for Neuroimmune Medicine, Nova Southeastern University, USA, has put
together a large multidisciplinary team, led by two ‘Blue Ribbon Fellowship’
medical students, who are concentrating on the genetic component, aiming to
understand the genetic risk in ME/CFS and the possible role of gene mutations.
This global study could help to provide a ‘genetic signature’ for ME/CFS and
explain why some people recover from ME/CFS and others do not.

From the Karolinska Institute,
Sweden, Dr Jakob Theorell’s research focuses on people who have
immunodeficiency syndromes. In relation to ME/CFS, he has been looking at a
specific part of the immune system orchestra called cytotoxic lymphocytes.
These are cells that combat intracellular infections with dysfunctional
abnormalities being reported in previous research studies.

Fane Mensah, PhD student at
University College London presented a summary of key points from a paper which
has reviewed the immunology of ME/CFS. The most consistent abnormality to be
reported in ME/CFS is a decrease in number and function of NK (natural killer)
cells. Studies that have looked at cytokines (immune system chemicals) have
produced inconsistent results. However, there is some evidence of changes in
the cytokine make up in relation to illness duration.

Dr Jo Cambridge, Professorial
Research Assistant at University College London, belongs to a well established
research group at UCL that has a particular interest in drug treatment
(rituximab in particular) relating to the depletion of a component of the
immune system orchestra called B cells. The group has also been exploring how B
cell depletion helps to modify the disease process in rheumatoid arthritis
through removing immune complexes and reducing inflammation in the joints.

Professor Simon Carding, Leader
in Gut Health and Food Safety Programme a the Institute of Food Research,
Norwich Research Park introduced four PhD students who are looking at
components of a research hypothesis that involves the gut.

Professor Mady Hornig, Associate
Professor, Centre for Infection and Immunity, Columbia University Mailman
School of Public Health, New York: Professor Hornig’s research focuses on
infective, immune and toxicstimuli
relating to conditions that range from autism to ME/CFS. She has a particular
interest in establishing how genes and maturational factors can interact with
environmental triggers, leading to various brain disorders. Her ME/CFS research
has concentrated on establishing whether there are immune system
profiles/signatures that are characteristic of the disease and identifying
infections that are linked to ME/CFS.

Professor Olav Mella, Dept.
Director, Oncology, Haukeland University Hospital, University of Bergen,
Norway: Professor Mella spoke on the current state of two separate clinical
trials in Norway involving rituximab and cyclophosphamide, looking back at how rituximab,
a drug that is normally used in cancer treatment, became a possible treatment
for ME/CFS. As an oncologist, his interest in the use of this drug in ME/CFS
occurred after three patients with lymphoma, who also had ME/CFS, noticed that
their ME/CFS significantly improved whilst receiving rituximab.

Dr Ingrid Rekeland, Dept of
Oncology, Haukeland University Hospital, University of Bergen, Norway: Dr
Rekeland is investigating whether there is a metabolic obstruction in the
pathway that creates glucose into energy inside the mitochondria and whether
this could help to explain some of the key symptoms of ME/CFS and the rise in
lactic acid production on exertion in some people with ME/CFS.

Professor Warren Tate, Group
Leader, Biochemistry Department, School of Biomedical Sciences, University of
Otago, New Zealand, opened his presentation by explaining that his research
interest in ME/CFS research resulted from his daughter developing the illness
at the age of 14. This followed an episodeof Epstein-Barr infection/glandular fever almost 20 years ago. He
likened the cause of ME/CFS to a large jigsaw puzzle where we had only some of
the pieces in place.

Professor Ron Davis, Professor of
Biochemistry and Genetics, Stanford School of Medicine, California, USA, is
also involved in ME/CFS research as a result of having a seriously ill son. He
updated the meeting on his research that is looking at the molecular basis to
ME/CFS, how this should help to increase both our understanding of the
underlying disease process and how this information can then be used to provide
effective forms of treatment.

We have made Dr Shepherd’s full
(16-page) conference report available as a download, which might make it easier
for people with M.E. to read at their own pace.

Thursday, 17 August 2017

Meditate a little on this mercy
of the Lord. It is tender mercy. With gentle, loving touch, He healeth the
broken in heart, and bindeth up their wounds. He is as gracious in the manner
of His mercy as in the matter of it. It is great mercy. There is nothing little
in God; His mercy is like Himself-it is infinite. You cannot measure it. His
mercy is so great that it forgives great sins to great sinners, after great
lengths of time, and then gives great favours and great privileges, and raises
us up to great enjoyments in the great heaven of the great God. It is
undeserved mercy, as indeed all true mercy must be, for deserved mercy is only a
misnomer for justice. There was no right on the sinner's part to the kind
consideration of the Most High; had the rebel been doomed at once to eternal
fire he would have richly merited the doom, and if delivered from wrath,
sovereign love alone has found a cause, for there was none in the sinner
himself. It is rich mercy. Some things are great, but have little efficacy in
them, but this mercy is a cordial to your drooping spirits; a golden ointment
to your bleeding wounds; a heavenly bandage to your broken bones; a royal
chariot for your weary feet; a bosom of love for your trembling heart. It is
manifold mercy. As Bunyan says, "All the flowers in God's garden are
double." There is no single mercy. You may think you have but one mercy,
but you shall find it to be a whole cluster of mercies. It is abounding mercy.
Millions have received it, yet far from its being exhausted; it is as fresh, as
full, and as free as ever. It is unfailing mercy. It will never leave thee. If
mercy be thy friend, mercy will be with thee in temptation to keep thee from
yielding; with thee in trouble to prevent thee from sinking; with thee living
to be the light and life of thy countenance; and with thee dying to be the joy
of thy soul when earthly comfort is ebbing fast.

Monday, 7 August 2017

When it comes to my illness, I've learned to listen to my symptoms, trust my body, and give it the one thing it really needs: rest.

Posted on August 6, 2017, at 10:46 a.m.

Camilla Maxted

It took 11 medical appointments across 20 weeks of pain and despair before I finally got a diagnosis.

For months, I’d been suffering from exhaustion so extreme that bit by bit, I’d had to let my whole life drop away. For a long time I tried to ignore it – after all, who stops doing anything just because they're tired? – but life became simply impossible. So first I cut down on my activities – like going for a run or seeing my friends – then, as my condition got worse, I cut them out completely. As for my job, I tried working from home, and I tried working half days. But my body just wouldn't play ball, and I had to stop working completely.

The tiredness was on a par with the worst flu you've ever had: Remember trying to drag yourself to the bathroom, or being hungry but barely strong enough to make food? As well as the fatigue, there were all sorts of aches and pains: a soreness in my spine, headaches and heavy limbs.

But this had lasted way longer than any flu. And now, here I was. After many fruitless discussions with GPs and inconclusive tests, I was finally in front of a specialist. He’d been able to put a clear label on my illness: a diagnosis of chronic fatigue syndrome. And he was now telling me that he had a track record of helping patients to recover. I nearly wept at my good fortune.

The doctor gave me an exercise program. “We’ll start small and build up from there,” he told me. “Stick to the routine and you'll see results.” He also said it was important that I stayed positive and didn't get too "lost" in my symptoms. “Try not to give them too much space in your mind, because you run the risk of magnifying them.”

-----------------------------------------------

The exercise started at a level I was comfortable with: five minutes of walking each day for the first week. At week two, five minutes became six, and so on. But by week four the nonstop walking had gotten to be too much. Weirdly, I was OK while doing the actual walk itself; it would hit me afterwards and I'd have to lie down, and I'd wake the next day feeling as though I'd run a marathon.

I discussed it with the doctor. “You're deconditioned,” he said. “You've been resting too much. Don't be afraid of exercise – it's good for you.”

I knew this made sense; exercise is good for you, isn't it? Besides, the doctor was a specialist – he'd seen it all before and he was assuring me this was the way to get better.

“I'll keep going,” I said.

“That's the right attitude,” said the doctor. He also reminded me not to dwell on my symptoms.

I didn't think I was dwelling. But when you have to lie down for days on end, it's hard to stay positive and upbeat, and it's hard not to think about the pain you're in. So I carried on walking, and hurting, and trying not to think about the hurting, and walking some more.

By week six, I had fallen behind on the programme and was feeling worse than ever. But the doctor told me that I wasn't trying hard enough. So I kept trying, and I kept paying the penalty. I didn't know what else to do, and it didn't occur to me that a doctor could consistently deny a patient’s reality. I thought maybe if I just tried a little harder, pushed a little further, I could prove the doctor right – and my own body wrong.

Going into week eight, I knew that I needed to stop. But I didn't want to give up. I held on and on to the hope of improvement – I didn't want to let my chance of recovery go. And I didn't want to stop and admit, even though by now it was clear, that not only was I not going to recover this way, but the treatment to which I'd so diligently applied myself had been making me worse.

I didn’t want to admit that, but eventually I had no choice. And when, one morning, I couldn't even make it to the kitchen to make my cup of coffee – let alone shower or dress – it was a relief to let it all go. Relief not simply because I could stop hurting, but because I could stop hurting myself. And with that I could cease the huge mental effort of trying to convince myself, in the face of all evidence, that I had been doing the right thing.

It soon became clear just how much I’d been fooling myself, as the payback for my efforts set in. Even now, even when I’ve experienced that same state of body and mind many times, it’s hard to convey what it’s like to be that sick. Hard to convey the crushing weight on my chest and limbs. Hard to convey the soreness, the shivers and the burning, the headaches, the other aches; the inability to concentrate on anything other than the feeling that every atom of my being was somehow spewing poison.

For several weeks, I was too sick to make it to the clinic, so my last conversation with the doctor was by telephone. And he didn’t seem particularly surprised or concerned to hear I’d decided not to return in person.

“I really urge you to have another go at some point,” were his parting words, as though it was simply a matter of my mustering the motivation. “That is,” he added, “if you really do want to get better.”

I hung up with the impression that, contrary to what I'd been told at the start, failures weren't so uncommon. I felt I was being shunted off the books, like a low-achieving pupil being excluded so that the school could maintain its high pass rate.

------------------------------------------

It turns out that the only thing more scary than developing a life-changing disease is finding that there is no effective help available. Reality drops away from you. Nothing in your previous life carries any weight any longer; nothing can give you strength or sense; all is swallowed into an enormous void, and the void is waiting for you, and it says: You’re on your own, and there is no resisting me.

After the worst phase of physical punishment for my efforts had passed, I also found that I'd lost the little function that I'd had before starting the exercise program. And when you get as bad as I was then, you become unable to advocate for yourself. You can’t leave your bed, and even if you could, you can’t hold a conversation in real time, because your brain won’t process things quickly enough.

There I lay, abandoned by the medical establishment – or had I abandoned it? Either way, I was full of fear, and the self-doubt instilled in me by the doctor remained. Should I try again, at some point? And what was going to become of me?

It was at that point, lost, alone, that I decided to do my own research. Sure, I’d done some light googling before, enough to find out that graded exercise was the only real option open to me (it was either that or cognitive behavioural therapy, designed to persuade me that I should think more positively and get active again – sound familiar?). But now I took a different approach, going beyond the official literature. I joined discussion forums, I started asking questions on social media, and, eventually, I learned to make sense of scientific papers.

As I dug deeper, I found that I wasn't alone in finding the exercise programme damaging. Around the world there were hundreds of thousands – possibly millions – of people stuck in their beds like me, and in the UK a sizeable proportion believed they had been put there by exercise therapy. And the rest of the world kept on spinning, and nobody knew.

From my bed, I learned that chronic fatigue syndrome, or CFS, is sometimes also known as myalgic encephalomyelitis, or ME. And I learned that the history of ME/CFS is a story of people bewildered, in pain, and often severely disabled, and suffering the even greater cruelty of being told their symptoms are only in their mind.

On the internet I met people who had been told they were “sick, not ill”. I met people who had been informed that “you must want to die, then”. (And I spoke to several who at times had felt that death would indeed be preferable.) I read the stories of children who had been removed from their families due to their parents’ refusal to force them to exercise.

I also met – online of course – several sufferers who had lived for months or years in darkness, unable to speak or interact, just strong enough to drink liquidised meals and drag themselves to the bathroom when necessary. But in this darkness I also found hope, support, and a sense of community.

I learned also that scientists had started to unpick the biological foundations of ME/CFS. Research groups in the US and Norway have now identified the disease as a sort of restricted metabolic state where the body can't manufacture energy in the normal way. No wonder exercise made me and so many others worse.

The science hasn't reached most doctors yet, but it will do. This means that help will, eventually, be on the way. Although there aren't yet any drug treatments for ME/CFS, some approaches have shown early promise.

Am I angry that I was given the wrong advice? Of course. And my heart breaks every time I read another story of how graded exercise put another person with ME/CFS in bed. More than this, though, I'm angry at how needlessly we have suffered. Why was biomedical research not begun earlier? Why were psychiatrists allowed to squash exploration in this field, by taking it and calling it their own? Why, even now, are people being told to undertake exercise programmes without being informed of the risks?

As for me, I am improving slowly, but it will be a long time before I can travel anywhere or work again. I've learned great patience, and even greater compassion for others; I'm truly thankful for that. These are qualities that will stay with me for life, because I have seen the cruelty and the grace of the world that we each experience, and the love that holds it all together.

And when it comes to my illness, I've learned to listen to my symptoms, trust my body, and give it the one thing it really needs: rest.

Inflammation biomarkers may help
doctors diagnose chronic fatigue syndrome (CFS), a poorly-understood condition
in which people feeling continually exhausted. These biomarkers could also give
new clues to what causes the condition, and how to treat it.

The biomarkers were discovered
when a team of researchers screened the blood of 192 people with chronic
fatigue syndrome for cytokines – substances used by the immune system to
control inflammation. The team compared the levels of 51 different cytokines in
the people with CFS and 392 people who didn’t have the condition, and found
that 17 cytokines rose in tandem with how bad a person’s CFS was.

“These 17 go up by various
degrees in a straight line with severity,” says José Montoya, of Stanford
University.

Overall, only one cytokine was
consistently higher in people with CFS. But when severity was taken into
account, the other 16 emerged from the analysis as being linked to the
condition. For example, three-times as much of the appetite hormone leptin, which
is part of the cytokine family, was present in people with very bad cases of
CFS.

Biological basis

It is not yet clear whether the
increase in inflammation markers could be a cause or result of the condition.

However, Montoya says the results
support mounting evidence that CFS is a physiological condition, not a
psychosomatic disorder. “There’s no question this is something that’s
biologically based,” he says. “This is a disease that does not get cured with
psychological treatments, counselling or anti-depression drugs.”

Montoya’s team want to use the
biomarkers to develop ways to diagnose CFS, also known as myalgic
encephomyelitis, and monitor its severity. These cytokines may also help
identify new CFS treatments that dampen inflammation, Montoya says.

“The results and how they were
obtained are encouraging, as finding markers for subsets and categorisations
within the illness is much needed for future research and treatments,” says
Chris Armstrong, of the University of Melbourne, Australia.

Dampening inflammation

Armstrong’s own team have found
that the fatigue of CFS may be caused by disrupted metabolism and energy production in the body. “The metabolic changes we found suggest a physiological
stressor in the body is affecting the cells,” he says. “The cause of that
stress is unknown, but is likely to be immune-based given the mounting evidence
in that direction – this new study included.”

I have cared full time, for 25
years, for my wife who has a diagnosis of Very Severe ME, my Nursing Standard
article "Supporting people with
severe myalgic encephalomyelitis" is referenced by NICE in the
original 2007 guidelines. In 2015 I was third place finalist, BJN, Nurse of the
Year, for which I received an award specifically for my work in raising
awareness of and advocating for people with Severe ME. I was Secretary of the
25% Severe ME Group charity for many years and represented the Group at the
Gibson Parliamentary Inquiry.

In February the Joint
Commissioning Panel for Mental Health document published Guidance for Commissioners of services for people with medically
unexplained symptoms – practical mental health commissioning, which misinformed
Commissioners that Myalgic Encephalomyelitis is a Somatoform, mental health
disorder.

The response, in a letter to me,
dated March 2nd, from the Co-Chairs of the Expert Reference Group for JCPMH
Guide on Commissioning for MUS and the Co-Chairs of the JCPMH claimed that the:
"The content of the MUS guide is
fully in line with NICE guidelines and with current practice. Should the
relevant NICE guidelines alter, or the evidence in this area change, then we
will revise the guide accordingly."

On March 15, NICE assured me that
CG53 does not list ME as a somatoform disorder. Therefore the MUS guidelines
cannot be correct.

I raised the misinformation in
the JCPMH Report with the Department of Health, who confirmed that the
Government recognises the WHO classification of ME as a neurological disease.
They advised me to take the issue up personally with you.

I am interested to know what you
can do to correct the misinformation that the JCPMH has given to Commissioners,
especially given the serious potential implication in regard to the current
consultation on CG53?

I also have the following
questions, given that NICE has confirmed that it does not consider ME to be a
Somatoform Disorder:

1. Can you tell me why NICE
itself lists ME under "Depression
and anxiety disorders" on the IAPT webpage and can you reassure me
that it will be removed? That surely is as great a misrepresentation of ME as
the JCPMH document, especially given the recognition in CG53 that “the physical symptoms can be as disabling as
multiple sclerosis, systemic lupus erythematosus and congestive heart failure .”

3. Can you tell me what role, if
any, IAPT played in the drafting of the recent CG53 Surveillance Document,
which has been heavily criticised by all major ME Charities and thousands of
patients for:

* its adherence to the widely
disputed CBT/GET paradigm, which has been shown to make patients, especially
the most severely affected, much worse. http://stonebird.co.uk/psurvey.pdf

* its many references to the universally
discredited PACE Trial

* its reliance upon vague
diagnostic criteria that do not clearly identify or separate ME from mental
health Chronic Fatigue (WHO F48). A wide definition helps no one; surely it is
time to acknowledge that ?

* its scant regard for biomedical
evidence

* its extraordinary decision not
to update the 10 year old guidance which not only was condemned as “unfit for
purpose” at the time, but continue to deny patients, like my profoundly
physically ill wife, equal access to health care

4. I am very curious to know the
composition of the Topic Experts and their knowledge base and impartiality.
What biomedical representation, if any, did you have? What clinical input,
outside of the biopsychosocial school, was involved for unbiased appraisal of
the biopsychosocial content? Can you tell me who the Topic Experts were? Were
any of the Royal College’s involved?

5. Can you tell me why NICE only
gave stakeholders two weeks to respond to the 56 page Surveillance document,
making it incredibly difficult for those people who have ME themselves or full
time carers, to have enough time to contribute adequately or at all.

6. Can you explain why NICE has
relied heavily on an unfounded psychiatric theory of ME that is nothing more
than that, with no real evidence itself, while ignoring the more than 9000
published papers that have been published world wide, detailing the biomedical
abnormalities in ME?

7. Can you explain, given the
statement in 2014 by Professor Mark Baker, Director of the Centre for Clinical
Practice, at a Forward- ME meeting, that the Guideline failed to address the real issues in ME/CFS, does not promote
innovation and has had a disappointing impact on specialist care and
commissioning issues, why NICE has continued to stick to its outmoded,
inappropriate, dangerous guidance?

The Surveillance document does
nothing, in my opinion, to challenge the misperception that ME is a mental
illness, in fact it's decision to come off the static list, not for medical
reasons, but because of the FITNET CBT/GET Trial reinforces the apparent
psychosocial bias of the whole document and attitude of NICE.

If CG53 continues to contribute
to a situation where people with ME are:

* misinterpreted as having a
mental health issue

* where biomarkers are not sought
for and relevant tests are proscribed

* where health professionals of
every level are misinformed and their awareness skewed wrongly towards a
biopsychosocial interpretation of a serious physical disease with ignored
multi-system dysfunction, endangering lives and leading to mistreatment,
misinterpretation, neglect and harm

* where ME is still not separated
from and confused with mental health Chronic Fatigue and other poorly diagnosed
diseases

* where services are geared
towards a psychiatric diagnosis of wrong illness thought and deconditioning

* where patients are offered
treatments that are inhuman, cruel, inappropriate and dangerous, because they
are in direct denial of their physical reality- the potential for harm is
enormous and terrifying in ME

then surely that is in
contravention of your obligations under the Human Rights Act and the Equality
Act?

The ME Community has been
insisting for years that CG53 is not and never has been appropriate for
patients with Myalgic Encephalomyelitis; the way forward is for ME to have its
own biomedical Guideline and pathway, categorically without psychiatric
interpretation and involvement.

About Me

I am a Christian, saved by grace alone through faith alone. I have had the neuroimmune disorder ME, Myalgic Encephalomyelitis, since 1991. From North Somerset, now in N. Ireland. Please see my website for further information about ME.